General Anesthesia Practice Questions

Q: A patient is posted for surgery 6 weeks post-burn. What is a likely cause of increased intraoperative requirements?

Succinylcholine. ### Explanation **Correct Answer: A. Succinylcholine** The correct answer is **Succinylcholine**, though the question phrasing "increased requirements" refers to the **increased risk/complication** associated with its use in the post-burn period. **Underlying Medical Concept:** In the post-burn state (typically from 24 hours up to 1–2 years post-injury), there is a massive **upregulation of extrajunctional acetylcholine receptors (nAChR)** across the muscle membrane. When Succinylcholine (a depolarizing neuromuscular blocker) is administered, these receptors open simultaneously, causing an efflux of potassium from the cells. In burn patients, this leads to **exaggerated hyperkalemia**, which can result in fatal cardiac arrhythmias or cardiac arrest. Therefore, Succinylcholine is strictly contraindicated in this period. **Why other options are incorrect:** * **B. Anesthetic negligence:** While complications can arise from errors, the physiological response to Succinylcholine in a burn patient is a known pharmacological phenomenon, not a result of negligence. * **C. Post-burn state:** While the "post-burn state" is the *reason* for the physiological change, it is not the "requirement" or the drug causing the specific intraoperative crisis mentioned in the context of anesthesia pharmacology. **High-Yield Clinical Pearls for NEET-PG:** * **The "Safe Window":** Succinylcholine is generally considered safe within the first **24 hours** post-burn. The risk of hyperkalemia peaks between **1 to 6 months** but can persist for over a year. * **Resistance to Non-depolarizers:** Conversely, burn patients show **resistance** to non-depolarizing muscle relaxants (e.g., Vecuronium, Rocuronium) due to the same receptor upregulation, requiring **increased doses** of these specific drugs. * **Potassium Shift:** A normal dose of Succinylcholine usually raises serum $K^+$ by **0.5 mEq/L**; in burn patients, this rise can exceed **5–10 mEq/L**.

Q: Which of the following drugs is known to cause severe pain on injection?

Thiopentone. **Explanation** The correct answer is **Thiopentone (Option A)**. **Why Thiopentone is correct:** Thiopentone sodium is an ultra-short-acting barbiturate used for the induction of anesthesia. It is highly alkaline, with a **pH of approximately 10.5**. Due to this high alkalinity, it is extremely irritating to the vascular endothelium. If injected into a small vein or accidentally administered **intra-arterially**, it causes intense pain, severe vasoconstriction (vasospasm), and can lead to tissue necrosis or gangrene. To minimize pain and the risk of thrombophlebitis, it is typically administered in a dilute concentration (2.5%). **Why the other options are incorrect:** * **Pethidine (Option B):** While pethidine can cause local histamine release leading to redness or itching along the vein, it is not primarily known for "severe pain on injection" in the same clinical context as alkaline barbiturates. * **Phenobarbitone (Option C):** Although also a barbiturate, it is a long-acting sedative/anticonvulsant. While alkaline, it is not the classic "high-yield" answer associated with induction-related injection pain in anesthesiology exams compared to Thiopentone or Propofol. * **Ketamine (Option D):** Ketamine is generally non-irritating to the veins and is often used in pediatric or emergency settings because it can be given intramuscularly without causing significant tissue damage or severe pain. **Clinical Pearls for NEET-PG:** * **Propofol** is the other common induction agent notorious for pain on injection (mitigated by using larger veins or pre-treating with Lidocaine). * **Management of Intra-arterial Thiopentone:** If accidental intra-arterial injection occurs, the needle should be left in place to administer vasodilators (e.g., **Papaverine** or **Phentolamine**) and a sympathetic block (e.g., Stellate ganglion block) to prevent gangrene. * **Etomidate** also causes significant pain on injection and a high incidence of myoclonus.

Q: Which inhalational agent acts on the NMDA receptor?

Xenon. **Explanation:** The mechanism of action for most volatile inhalational anesthetics primarily involves the enhancement of inhibitory neurotransmission via **GABA-A receptors**. However, a specific group of anesthetic gases works by inhibiting excitatory neurotransmission, specifically by acting as **non-competitive antagonists at the N-methyl-D-aspartate (NMDA) receptor**. **Why Xenon is correct:** Xenon is an inert gas that produces anesthesia by binding to the glycine site of the NMDA receptor, thereby inhibiting it. This unique mechanism contributes to its remarkable profile: it provides rapid induction and emergence (due to an extremely low blood-gas partition coefficient of 0.115), offers significant neuroprotection, and maintains hemodynamic stability. Other agents that share this NMDA-antagonist mechanism include **Ketamine** and **Nitrous Oxide (N₂O)**. **Why other options are incorrect:** * **Options B, C, and D (Desflurane, Sevoflurane, Isoflurane):** These are halogenated ethers (volatile liquids). Their primary molecular target is the **GABA-A receptor**, where they increase chloride conductance, leading to hyperpolarization of the postsynaptic neuron and CNS depression. While they may have minor effects on other channels, they are not classified as primary NMDA antagonists. **High-Yield Clinical Pearls for NEET-PG:** * **Ideal Anesthetic:** Xenon is often called the "ideal anesthetic" because it is non-explosive, non-toxic, and has minimal cardiovascular side effects. * **Blood-Gas Partition Coefficients:** Xenon (0.115) < Desflurane (0.42) < Nitrous Oxide (0.47) < Sevoflurane (0.65) < Isoflurane (1.4). * **MAC of Xenon:** Approximately 63–71%, making it less potent than volatile liquids but more potent than Nitrous Oxide. * **Key NMDA Antagonists in Anesthesia:** Xenon, Nitrous Oxide, Ketamine, and Magnesium.

Q: Which of the following drug(s) is/are mainly metabolized extrahepatically in plasma?

Atracurium. **Explanation:** The correct answer is **Atracurium**. **1. Why Atracurium is correct:** Atracurium is a non-depolarizing neuromuscular blocking agent unique for its metabolism. It undergoes **extrahepatic metabolism** via two primary pathways: * **Hofmann Elimination:** A spontaneous, non-enzymatic degradation that occurs at physiological pH and temperature. * **Ester Hydrolysis:** Catalyzed by non-specific plasma esterases (Note: This is distinct from pseudocholinesterase). Because it does not rely on the liver or kidneys for clearance, it is the drug of choice in patients with **hepatic or renal failure**. **2. Why the other options are incorrect:** * **Halothane:** An inhalational anesthetic primarily eliminated via the lungs, but approximately 20% undergoes **oxidative metabolism in the liver** by CYP450 enzymes. This metabolism is linked to "Halothane Hepatitis." * **Propofol:** An intravenous anesthetic primarily metabolized in the **liver** (conjugation to glucuronides). While it has some extrahepatic clearance (lungs), the liver remains the chief site. * **Lignocaine:** An amide local anesthetic that is almost entirely metabolized by **hepatic microsomal enzymes** (dealkylation). Its clearance is highly dependent on hepatic blood flow. **3. High-Yield Clinical Pearls for NEET-PG:** * **Cisatracurium:** An isomer of atracurium that undergoes *only* Hofmann elimination. It is more potent and produces less **laudanosine** (a metabolite of atracurium that can trigger seizures) and less histamine release. * **Mivacurium:** The only non-depolarizing muscle relaxant metabolized by **pseudocholinesterase** (butyrylcholinesterase), similar to Succinylcholine. * **Remifentanil:** An opioid also notable for extrahepatic metabolism via non-specific tissue and plasma esterases, giving it an ultra-short duration of action.

Q: RBC infusion is not done with which of the following solutions?

Ringer's Lactate (RL). **Explanation:** The correct answer is **Ringer's Lactate (RL)**. The primary reason RL is contraindicated for co-administration with Packed Red Blood Cells (PRBCs) is its **calcium content**. Ringer’s Lactate contains ionized calcium (approximately 3 mEq/L). Blood products are typically anticoagulated with **Citrate**, which works by chelating calcium to prevent the clotting cascade. When RL is mixed with citrated blood, the calcium in the RL overcomes the anticoagulant effect of the citrate, leading to the formation of **microclots** within the infusion tubing or the blood bag. These clots can cause fatal pulmonary embolism if infused. **Analysis of Options:** * **Normal Saline (0.9% NaCl):** This is the **fluid of choice** for blood transfusion. It is isotonic and contains no calcium, making it safe to use for priming tubing or diluting PRBCs to decrease viscosity. * **5% Dextrose:** While it contains no calcium, it is **avoided** because it is hypotonic once the glucose is metabolized. This causes water to move into the RBCs (osmosis), leading to swelling and **hemolysis**. * **Normosol:** This is a balanced salt solution that is **calcium-free** (it uses magnesium instead). Therefore, it is compatible with blood products and does not cause clotting. **High-Yield Clinical Pearls for NEET-PG:** * **Plasmalyte A** is another calcium-free balanced salt solution that is safe for blood transfusion. * **Citrate Toxicity:** Rapid transfusion of multiple units can lead to hypocalcemia (as citrate binds the patient's endogenous calcium), manifesting as a prolonged QT interval on ECG. * **Ideal Ratio:** If dilution is needed to improve flow rates in emergencies, 0.9% NS is the only standard recommendation.

Q: Which of the following anesthetic agents has the least cardiovascular side effects?

Isoflurane. **Explanation:** **Isoflurane** is considered the gold standard among volatile anesthetics for cardiovascular stability. While it causes a dose-dependent decrease in systemic vascular resistance (SVR) leading to a drop in blood pressure, it uniquely **preserves cardiac output**. This is because the decrease in SVR is compensated by a mild increase in heart rate (baroreceptor reflex). Unlike other halogenated agents, it does not significantly depress myocardial contractility, making it safer for patients with compensated heart disease. **Why other options are incorrect:** * **Enflurane:** It causes significant myocardial depression and a greater reduction in cardiac output compared to Isoflurane. It is also associated with a higher risk of arrhythmias and can lower the seizure threshold. * **Trilene (Trichloroethylene):** It is highly arrhythmogenic, especially in the presence of endogenous or exogenous catecholamines (sensitizes the myocardium to adrenaline). It is no longer used in modern anesthesia due to toxicity. * **Ketamine:** While it is often used in hemodynamically unstable patients, it is **not** free of cardiovascular side effects. It is a potent sympathomimetic that causes significant increases in heart rate, blood pressure, and myocardial oxygen demand, which can be detrimental in patients with coronary artery disease. **High-Yield Clinical Pearls for NEET-PG:** * **Coronary Steal Phenomenon:** Classically associated with Isoflurane (theoretical), where it dilates small coronary arterioles, potentially diverting blood away from ischemic areas. * **Drug of Choice for Neurosurgery:** Isoflurane is preferred as it maintains cerebral blood flow autoregulation better than other older agents. * **Halothane:** Most likely to cause "Halothane Hepatitis" and myocardial sensitization to catecholamines. * **Sevoflurane:** Agent of choice for **inhalational induction** due to its non-pungent nature and low blood-gas solubility.

Q: Which anaesthetic agent is known to produce adrenocortical suppression in a patient with Cushing's syndrome undergoing surgery?

Etomidate. **Explanation:** **Etomidate** is a carboxylated imidazole derivative used for induction of anesthesia. It is uniquely associated with **adrenocortical suppression** because it causes dose-dependent inhibition of the enzyme **11-beta-hydroxylase**. This enzyme is essential for converting 11-deoxycortisol to cortisol. Even a single induction dose can suppress cortisol production for 6 to 24 hours. While this side effect is generally undesirable in trauma or septic patients, it can be pharmacologically exploited in patients with **Cushing’s syndrome** to temporarily reduce excessive cortisol levels during the perioperative period. **Analysis of Incorrect Options:** * **Thiopentone (A):** An ultra-short-acting barbiturate. Its primary side effects are cardiovascular and respiratory depression; it has no specific inhibitory effect on the adrenal cortex. * **Ketamine (C):** A dissociative anesthetic that acts as a sympathetic stimulant. It actually increases plasma cortisol levels by stimulating the hypothalamic-pituitary-adrenal axis, making it the opposite of etomidate. * **Propofol (D):** The most common induction agent. While it can cause hypotension due to vasodilation, it does not interfere with steroidogenesis. **High-Yield NEET-PG Pearls:** * **Drug of Choice:** Etomidate is the induction agent of choice for patients with **compromised cardiovascular status** (e.g., valvular heart disease, CAD) because it is hemodynamically stable. * **Myoclonus:** Etomidate frequently causes involuntary muscle movements (myoclonus) on induction, which can be prevented by premedication with opioids or benzodiazepines. * **Nausea/Vomiting:** It has a high incidence of Postoperative Nausea and Vomiting (PONV). * **Contraindication:** Strictly avoided in patients with **Addison’s disease** or severe sepsis due to its adrenal suppressive effects.

Q: What is the recommended dose of thiopental sodium?

3-5 mg/kg. **Explanation:** **Thiopental Sodium** is a short-acting thiobarbiturate used primarily for the induction of general anesthesia. The correct induction dose is **3–5 mg/kg** intravenously in healthy adults. 1. **Why 3–5 mg/kg is correct:** This dosage range is calculated to achieve a rapid loss of consciousness (within 30–45 seconds) by crossing the blood-brain barrier quickly due to its high lipid solubility. It acts by facilitating GABA-A receptors, increasing the duration of chloride channel opening, which leads to CNS depression. 2. **Why other options are incorrect:** * **1–2 mg/kg:** This is an under-dose for induction in healthy adults but may be used in elderly patients or those in hypovolemic shock, as thiopental can cause significant myocardial depression and peripheral vasodilation. * **5–10 mg/kg & 10–15 mg/kg:** These doses are excessively high and would lead to prolonged apnea, severe hypotension, and delayed emergence due to the drug's cumulative effects and saturation of redistribution sites. **High-Yield Clinical Pearls for NEET-PG:** * **Redistribution:** The rapid recovery from a single bolus of thiopental is due to **redistribution** from the brain to lean tissues (muscle), not metabolism. * **pH & Solubility:** It is highly alkaline (pH 10.5). Accidental **intra-arterial injection** causes severe vasospasm and gangrene; treatment includes papaverine, lidocaine, or a sympathetic block. * **Contraindication:** It is strictly contraindicated in **Porphyria** (induces ALA synthetase). * **Context-Sensitive Half-life:** It has a long context-sensitive half-life, making it unsuitable for maintenance via infusion.

Question 1

A patient is posted for surgery 6 weeks post-burn. What is a likely cause of increased intraoperative requirements?

Accepted Answer

Succinylcholine

Answer

Anesthetic negligence

Answer

Post-burn state

Answer

None of the above

Question 2

Which of the following drugs is known to cause severe pain on injection?

Accepted Answer

Thiopentone

Answer

Pethidine

Answer

Phenobarbitone

Answer

Ketamine

Question 3

Which inhalational agent acts on the NMDA receptor?

Accepted Answer

Xenon

Answer

Desflurane

Answer

Sevoflurane

Answer

Isoflurane

Question 4

All are true about the dosing of succinylcholine EXCEPT:

Accepted Answer

In obese patients, the dose is calculated according to lean body weight.

Answer

In adults, a dose of 1.0 mg/kg body weight can yield intubating conditions.

Answer

Children are resistant to succinylcholine, so between 1 to 2 mg/kg is required.

Answer

In infants, the dose is between 2-3 mg/kg.

Question 5

Which of the following drug(s) is/are mainly metabolized extrahepatically in plasma?

Accepted Answer

Atracurium

Answer

Halothane

Answer

Propofol

Answer

Lignocaine

Question 6

RBC infusion is not done with which of the following solutions?

Accepted Answer

Ringer's Lactate (RL)

Answer

Normal Saline (NS)

Answer

5% Dextrose

Answer

Normosal

Question 7

Which of the following anesthetic agents has the least cardiovascular side effects?

Accepted Answer

Isoflurane

Answer

Enflurane

Answer

Trilene

Answer

Ketamine

Question 8

Which anaesthetic agent is known to produce adrenocortical suppression in a patient with Cushing's syndrome undergoing surgery?

Accepted Answer

Etomidate

Answer

Thiopentone

Answer

Ketamine

Answer

Propofol

Question 9

A 65-year-old male with a history of acute onset vomiting and weight loss was diagnosed with stomach carcinoma and a Whipple's procedure was planned. Preanesthetic evaluation revealed deranged kidney function. Which inhalational agent is the agent of choice?

Accepted Answer

Desflurane

Answer

Sevoflurane

Answer

Halothane

Answer

Isoflurane

Question 10

What is the recommended dose of thiopental sodium?

Accepted Answer

3-5 mg/kg

Answer

5-10 mg/kg

Answer

1-2 mg/kg

Answer

10-15 mg/kg

General Anesthesia — MCQs

General Anesthesia — MCQs

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